STEPHEN Daniels's customers were treating the mad sheep scare as a bit
of a joke yesterday.
"People have been coming in and saying 'Oh, what am I allowed to eat
now?' Then they ask for lamb chops," said Mr Daniels

"We've had eggs, poultry, beef, now sheep - I think it's getting to the
stage where people are laughing at it all. When I saw it on television I
laughed too. I suppose there will be a turkey scare at Christmas."
But Mr Daniels, 43, who has run Artingstalls Family Butchers in Chipping
Sodbury for 10 years, doesn't always see the funny side of the never-
ending BSE crisis.

"It seems that all these scientists have done is take BSE from a beef
animal, inject it into a sheep, then say that sheep can get mad cow
disease," he said. "They don't seem to realise what damage they're doing
to the meat industry."
Margaret Harding came into Artingstalls to buy pork and apple sausages
and lamb's liver. "It's getting a bit silly now," she said. "What can we
eat and what can't we eat - does anyone know? I sometimes think we
should be more worried about what they spray on vegetables than about
meat."

Across the street at M. E. Nelson Family Butchers, Mike Nelson has
reacted to the series of food scares by diversifying. "My wife and my
son work here, it's our family business, so we had to sit down and
scratch our heads to decide how to keep going," he said. "We didn't used
to sell quiches and vegetables but we have to now. We're lucky because
we serve a farming community out here in the sticks. Every time BSE
reared its head the farmers supported us. Otherwise, we might have
closed like a lot of town butchers. There's been a lot of pressure,
maybe that's why I had a heart attack."

Sisters Anita Moore and Liz Herbert, shopping in the high street, said
they had continued to eat beef and would not worry about buying lamb
Mr Nelson, 57, believes his business has seen off the worst of the
problem partly because the public have more trust in small, independent
butchers than in anonymous supermarkets.

He said: "I'm hoping the public are going to get fed up with it -
they'll start asking themselves what can they eat. My wife will eat
salad every day, 365 days a year. But I need more substance."

Sisters Anita Moore and Liz Herbert, shopping in the high street, said
they had continued to eat beef and would not worry about buying lamb.
Mrs Moore said: "I think there's always a lot of scaremongering about
these things. Some of the publicity has been quite off-putting but my
impression was that we might have been at risk in the past, before they
identified the problem and the rules were put in place."

Mrs Herbert said: "I think it's important to have a lot of safeguards
with regard to our food in the first place. When these things come along
we're left wondering if they're the tip of the iceberg or just a storm
in a teacup? "
Jill Norris, 51, was having difficulty deciding what meat to buy. "I
bought cold meats in the end," she said. "I did look at the lamb chops
but I think my husband would end up saying no.

"Every time there's a scare he says 'don't give me any of that'. He
stopped eating eggs after that row and he stopped eating chicken. He
gave up beef after the last fuss.
"Then after he saw the news on television last night he said he was
going to become a vegetarian. So I don't know what we're going to eat."

A SURVEY to establish whether mad cow disease has spread to sheep is to
be conducted by the same team of scientists who established that BSE can
infect sheep.
"We have been building the experimental protocol of this survey for some
time but the results will not be known for a couple of years," said Prof
John Bourne, director of the Institute for Animal Health, at Compton,
near Newbury.

The team will take various pure-bred strains of mice and inject them
with contaminated tissue, then wait for disease to develop.
If a sheep sample has the same pattern of disease as one from a BSE-
infected cow, they are likely to be the same strain of spongiform
disease. "If we find it, it begs the question of where it came from,"
said Prof Bourne.

One possibility would be that BSE was transmitted by contaminated feed.
Another would be that it was the original scrapie that started the BSE
epidemic.
"The overall evidence suggests to us that the BSE problem did arise from
sheep scrapie," said Prof Bourne.

The alarm over contamination of the national flock by BSE was raised in
a paper in the Veterinary Record, by scientists at the Institute for
Animal Health's Neuropathogenesis Unit, in Edinburgh.
They found that BSE can be transmitted to sheep by injecting
contaminated cow tissue directly into the brains of animals and also by
contaminated feed.

The disease is linked to a brain protein, called prion protein. The
experimentally infected sheep showed that the agent maintained all the
hallmarks of BSE but the disease also affected the spleen as well as the
spinal cord and brain, as one would expect from scrapie.

By George Jones, Political Editor Daily Telegraph
Thursday July 25 1996

STRICTER controls on the slaughter of sheep were proposed by the
Government yesterday after scientific evidence that BSE in cattle could
be transmitted to them.

Douglas Hogg, the Agriculture Minister, said the Government was
proposing that the heads of all sheep and goats be destroyed in the same
way as for cattle in the slaughter process. "These steps are being taken
out of an abundance of caution. There is no direct threat to human
health," he assured the Commons in a statement.

Mr Hogg also assured MPs there was no evidence that scrapie in sheep and
goats, a brain disease similar to BSE, was linked to Creutzfeldt Jakob
Disease in humans.
Gavin Strang, Labour's agriculture spokesman, backed the new measures,
saying it was right to "err on the side of caution".

Mr Hogg said the Spongiform Encephalopathy Advisory Committee (SEAC) had
advised that BSE "could, theoretically, become established in the sheep
flock". There was no evidence of BSE occurring naturally in the flock,
but the committee was concerned that scrapie might be "masking" BSE.
Mr Hogg said the Government was consulting its European partners and the
Commission was formulating proposals for the removal of certain offals
of sheep, goats and deer from the human and animal food chain.

On the recommendation of SEAC, agriculture officials had issued for
consultation a proposal that the heads of all sheep and goats be removed
and destroyed in the same way as cattle.
"It should not have a major economic impact as the vast majority of
sheep's heads are already destroyed. It is worth noting that sheep meat
for human consumption comes predominantly from young lambs under 12
months," said Mr Hogg.
"That's another fine mess you have got yourself into, or this industry
into"

"With the exception of the consumption of brains, there is absolutely no
reason for anybody to change their eating habits. I repeat: there is no
evidence at all that in field conditions BSE has got into the national
flock, but as that possibility cannot be wholly excluded we are
proposing to take these precautionary measures."
He said the Government was commissioning further research into the
possible transmission of BSE to the British sheep flock.

Paul Tyler, for the Liberal Democrats, said such precautionary measures
were irrelevant to the traditionally reared and butchered British lamb.
"Is it not true that the English chop is safe in our time?" he said.
To cheers from MPs, Mr Hogg said the British chop was "a splendid
product" that could be eaten in complete safety.
But John Robertson, Labour MP for East Lothian and a farmer, told Mr
Hogg: "That's another fine mess you have got yourself into, or this
industry into." The Government was driving consumers and producers to despair.

"Rohwer (in: Transmissible Spongiform Encephalopathies: Scrapie, BSE and
Related Human Disorders, ed. by B.W. Chesebro, Berlin, Heidelberg, New York,
London and so on, 1991) emphasizes too that CJD didn't exist in Slovakia in
former generations. I remember having read somewhere else (but where?) that
CJD started at a certain point in time with victims of different age.

Mayer, Orolin and Mitrova (The Lancet, July 30, 1977) report 10 CJD cases
between 1972 and 1977, in a clearly defined area; an extend not reported
before in Slovakia.
The Fore in New Guinea too could remember (according to Gajdusek) that Kuru had started at
a certain point in time (about 1920-1925), whereas the disease hadn't existed
before. Such a start is very typical of an infection which arrives at a region for
the first time.
According to the reports of the Gajdusek-group, already two four-year and
7-year-old children came down with kuru. They can have been infected as
toddlers (1 - 1.5 years) at the earliest. We have to assume that - like in
animal experiments with TSE - the outbreak of the disease was determined by
the dose of infection: more relatives dead of kuru - more infectious rituals
- earlier outbreak of kuru with the persons involved in the funeral rituals.

Women and children were also the only ones to eat infectious brain; men and
older boys were not involved. The dose of infection of women and younger
children might therefore have been substantially higher than that of knacker
men and renderer staff. On top of it, young children probably run the highest
risk: Taylor (Vet. Rec. 1989, 14, p. 413 ff.) proofed by animal experiments
that scarification in the oral cavity increases the risk of infection
significantly. Applied to men , this means that the agent could directly pass
into the blood system in case of second dentition and tonsillitis - thus the
incubation period would shorten.
We should also remember that 2 British abattoir workers (at the age of about
50) came down with CJD - probably with a different variation than the V-CJD
victims. Spontaneous CJD may be the result of an infection. It's unlogical to postulate
85% of the CJD cases as "causally unknown", whereas it is known at the same
time that all other TSE are infections (kuru included)."

UK Institute for Animal Health.
"The article below is at Babraham, Cambridge. There may be another at Compton, Berkshire.
The 1995 report gives details of some genetic lines conferring
resistance in Cheviot sheep. Note that this is a different breed than
the Suffolks mentioned in the magazine. However the authors may well
know of other work.

The scrapie genotype test costs UKP 70
PrP genotypes of sheep affected with natural scrapie and those of
healthy flock mates are being compared. Differences have
been noted between outbreaks and between flocks. This may be due to
differences in the strain of natural scrapie affecting the
flock or may reflect breed differences in the sheep themselves.
The most important variants of the PrP gene are those differing at codon
136 and 171. Valine at codon 136(V136) has a
dominant association with incidence of scrapie but is not found in all
breeds of sheep. Glutamine at codon 171 (Q171) has a
recessive association with scrapie and has been found in all breeds of
sheep examined so far.
The NPU Cheviot flock had 45 deaths from natural scrapie between 1986
and 1995. Of these cases 39 were analysed for
disease-linked PrP gene polymorphisms and all encode V136 on at least
one allele with 79% homozygous (VV136) and 21%
valine/alanine heterozygotes (VA136). Mean survival time was 888 and
1482 days for VV136 and VA136 animals respectively.
VV136 animals were all at great risk of disease if allowed to live long
enough. However, scrapie occurred only in a specific
subgroup of VA136 sheep, survival advantage depending on VA136 animals
being heterozygous for other polymorphisms at
codon 154 or 171.
The flock history has been recorded in great detail since its foundation
in 1960. However there was no strong evidence for
simple maternal or paternal transmission of disease other than
inheritance of PrP genotype.
In a Suffolk flock with scrapie, cases occurred in animals according to
their PrP genotype at codon 171. QQ171 sheep were at
great risk of scrapie whereas those which were arginine/glutamine
heterozygotes (RQ) were at less risk and RR171 animals
appeared to be resistant. A histidine codon (H171) can also be found at
this position in Suffolk sheep but this did not occur in
scrapie-affected animals.

Natural modes of transmission:
The incidence of natural scrapie in the NPU's flock of Cheviots is
linked to PrP genotype. The flock is maintained as two
breeding lines, one (susceptible: 'positive') which has endemic natural
scrapie and the other (resistant: 'negative') which is
entirely free from clinical manifestation of the disease.

The positive line is being bred to carry specific PrP genes which are
linked to susceptibility to experimental inoculation but
resistant to the natural disease (VA136/RQ171), thereby controlling its
incidence by manipulating genetic frequency. The negative
line is being bred for different PrP genes (AA136/RR171, RQ171, QQ171)
which also never allow natural scrapie to develop and
in which transmission experiments can be achieved without compromise. A
further line, completely segregated from the first
two, is being bred to generate an high incidence of natural scrapie, by
increasing the frequency of susceptible PrP genes